Congestive heart failure and dilated cardiomyopathies are just two conditions that result in the elongation of individual myocytes. The resulting hemodynamic disadvantages of significant ventricular dilatation (either right or left) can be overcome by progressive epicardial compression resulting in reduction of diastolic ventricular volume, increased ventricular contractility and improved cardiac output. Research has also shown that regression of fibrosis and hypertrophy occurs when loading is reduced on a failing heart (Bruckner, et al., 2001).
Patients that will receive particular benefit are those suffering from non-ischemic cardiomyopathy. These cases can be further stratified into dilated, hypertrophic and restrictive cardiomyopathy. The three classes describe differing muscle damage to the heart. The most common type is dilated cardiomyopathy. Myocytes are stretched due to some mechanism such as disease or increased workload. The elongated or hypertrophic myocytes lead to a dilated ventricle (either right or left). In what may be a misguided attempt to compensate for this state, such a heart will allow itself to become further stretched, inducing secondary focal ischemia, which in fact leads to further degradation of the heart's ability to perform (Robertson, 1999). Heart failure is the hallmark of dilated cardiomyopathy.
The inventor has studied the cellular physiology involved in compensation. In particular, the mechanisms of vasoconstriction, increased cardiac adrenergic drive, and the activation of transcription factors and their short term and long term implications that produce heart failure (Robertson). Also, compressive mechanical support of a dilated heart has been shown to reduce the cardiac workload. In a study using ventricular assist devices, reduced cardiac workload has shown regression of heart failure symptoms. Therefore, compressive mechanical support will reduce the condition of heart failure. Progressive control will afford optional recovery for an individual patient. In earlier research related to the treatment of arterial aneurysms, the idea of a progressive therapeutic support mechanism had shown clinical relevance in studies on animal models decades ago. With an understanding of the pathophysiology of congestive heart failure and of cardiomyopathy this approach is directly needed for safe and cost-effective treatment of the failing heart.
The device can be thought of in two parts. First, a cardiac enclosure affords a means of defining an upper limit on the cardiac geometry. This geometry can subsequently be adjusted through two or more highly elastic and/or highly conforming chambers or bladders that reside on the inside of the enclosure. The independent inflation of each chamber addresses the needs for specific progressive support of the individual ventricular diastolic volume. For example, in the case of congestive heart failure usually the right ventricle is predominantly dilated, inducing higher diastolic systemic pressure while not initially changing the geometry of the left ventricle to a substantial degree. In contrast, in left ventricular failure, usually following transmural myocardial infarction, or in dilated cardiomyopathies, progressive support is required for the left cardiac chamber to reduce ventricular volume. Eventually, in many cases, both ventricles may become dilated and require support.
At present no publications address the need for an easily adjustable, percutaneous, gas/liquid filled cardiac support device. Previous experimental and anatomopathological studies by the inventor have suggested the potential reversibility of heart failure by reducing elongation of individual ventricular myocardial fibers. This may also reduce the incidence of randomized programmed cell death or apoptosis and reverse losses of ventricular contractility.
In summary, the treatment of congestive heart failure and dilated cardiomyopathies, which involves over 500,000 new cases a year, in the U.S. alone, could be strongly impacted by such a device. It offers to the cardiothoracic surgeon the use of a customized progressive ventricular diastolic assist device requiring no external mechanical support, while allowing repeated percutaneous adjustments based on clinical and hemodynamic data that provides a novel solution to a large patient population.